Lupus erythematosus and lupus nephritis - Diagnosis

Laboratory diagnostics of lupus erythematosus and lupus nephritis

Laboratory tests for lupus nephritis are aimed at identifying signs of systemic lupus erythematosus and symptoms that characterize the activity of lupus nephritis and the state of kidney function.

Characteristic laboratory abnormalities include anemia, leukopenia with lymphopenia, thrombocytopenia, a sharp increase in ESR, hypergammaglobulinemia, the presence of LE cells, antinuclear factor and antibodies to native DNA, hypocomplementemia (a decrease in the total hemolytic activity of complement CH-50, as well as fractions C3 and C4).

The activity of lupus nephritis is judged by the severity of proteinuria, the presence of acute nephritic and/or nephrotic syndromes, the nature of urinary sediment, and deterioration of renal function (increased creatinine concentration in the blood and decreased SCF).

Differential diagnosis of lupus erythematosus and lupus nephritis

In the case of a full-blown clinical picture of systemic lupus erythematosus, the diagnosis of lupus nephritis is practically not difficult. The diagnosis is established in the presence of any 4 or more of the 11 diagnostic criteria of the American Society of Rheumatology (1997).

• Erythema of the face ("butterfly").
• Discoid rash.
• Photosensitivity.
• Cheilitis, oral ulcers.
• Nonerosive arthritis.
• Serositis (pleurisy, pericarditis).
• Kidney damage (proteinuria more than 0.5 g/day and/or hematuria).
• Neurological disorders (seizures or psychosis).
• Hematological disorders (hemolytic anemia, leukopenia and/or lymphopenia, thrombocytopenia).
• Increased titer of antibodies to DNA, presence of antibodies to Sm-Ar, antiphospholipid antibodies (including IgG and IgM antibodies to cardiolipin or lupus anticoagulant).
• Positive antinuclear factor test.

Differential diagnostics of lupus nephritis is carried out with other systemic diseases that occur with kidney damage: nodular polyarteritis, Henoch-Schonlein purpura, drug disease, autoimmune hepatitis, rheumatoid arthritis, myeloma, infections (subacute infective endocarditis, tuberculosis). In case of erased systemic manifestations, it is necessary to differentiate lupus nephritis from chronic glomerulonephritis. In these cases, a kidney biopsy can be invaluable, since histological examination of the obtained material can reveal specific morphological signs of lupus nephritis.

• Polyarteritis nodosa, unlike systemic lupus erythematosus, develops predominantly in men aged 30-50 years and occurs with peripheral asymmetric polyneuritis, abdominalgia, coronary artery disease, and leukocytosis. Kidney damage in polyarteritis nodosa is manifested by vasculitis of the renal vessels with the development of persistent, often malignant arterial hypertension with moderate urinary syndrome (proteinuria, often combined with microhematuria). Nephrotic syndrome is extremely rare.
• Kidney damage in Henoch-Schonlein purpura (hemorrhagic vasculitis) is often combined with damage to large joints, skin (characterized by recurrent symmetrical hemorrhagic rashes on the shins, buttocks, elbows), and abdominal pain syndrome. Children and adolescents are more likely to get sick, often after a respiratory infection. Nephritis, as a rule, occurs with macrohematuria, which is unusual for systemic lupus erythematosus, and a high level of IgA in the blood.
• A clinical picture similar to lupus nephritis may occur in rheumatoid arthritis with kidney damage, especially in the presence of other systemic manifestations (lymphadenopathy, anemia, lung damage). However, rheumatoid arthritis is characterized by a long course of the disease with the development of persistent joint deformities, pronounced radiographic changes (erosive arthritis), high titers of rheumatoid factor in the blood (in systemic lupus erythematosus, rheumatoid factor in the blood is noted infrequently and in low titers). In kidney biopsy, amyloid is detected in more than 30% of patients, which is practically not detected in systemic lupus erythematosus.
• It is sometimes difficult to differentiate lupus nephritis from kidney damage in drug-induced disease, as well as in autoimmune hepatitis, due to the numerous systemic manifestations characteristic of these diseases, as well as systemic lupus erythematosus.
  • Kidney damage in drug-induced disease often occurs as interstitial nephritis, a characteristic feature of which, in addition to moderate urinary syndrome and acute renal failure of varying severity, is considered to be tubular disorders, manifested primarily by a decrease in the relative density of urine. Morphological examination reveals a predominance of changes in the tubules and interstitium.
  • In autoimmune hepatitis, nephritis is rarely accompanied by massive proteinuria; the tubulointerstitial component is most characteristic, often with pronounced tubular dysfunctions. Signs of serious liver damage are of decisive differential diagnostic importance.
• Differential diagnostics of lupus nephritis with myeloma nephropathy is performed in women over 40 years of age with a sharply increased ESR, anemia, bone pain in combination with massive proteinuria without the formation of nephrotic syndrome or progressive renal failure. Myeloma disease is confirmed by X-ray examination of flat bones, immunoelectrophoresis of blood and urine proteins, sternal puncture. Kidney biopsy is undesirable if myeloma disease is suspected due to the risk of bleeding.
• For patients with systemic lupus erythematosus, differential diagnosis of lupus nephritis with infections requiring massive antibacterial therapy, primarily with subacute infective endocarditis and tuberculosis with paraspecific reactions, is extremely important.
  • Subacute infective endocarditis is accompanied by fever, leukocytosis, less often leukopenia, anemia, increased ESR, heart damage, and sometimes kidney damage. Nephritis is often hematuric in nature, but nephrotic syndrome and even rapidly progressive glomerulonephritis may develop. An important differential diagnostic sign is the formation of aortic insufficiency, which extremely rarely develops with Libman-Sachs endocarditis in patients with systemic lupus erythematosus. "Minor" signs of subacute infective endocarditis are of important differential diagnostic value: symptoms of drumsticks and watch glasses, Lukin-Libman sign, positive pinch symptom. In doubtful cases, blood culture and trial treatment with high doses of antibacterial drugs are necessary.
  • It is equally important to exclude tuberculosis (which may join lupus nephritis after massive immunosuppressive therapy).

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